AN EXPERIMENTAL INVESTIGATION OF MULTI-CYLINDER CONVENTIONAL CI ENGINE USING MADHUCA INDICA OIL AS FUEL

The present work is mainly discussed with a qualitative study of engine’s significant characteristics fuelled with mahua bio-diesel & its different types of mixtures with neat diesel. The significant technical properties of various mixtures are tabulated. A 4-S multi-cylinder (6-Cylinder) DI conventional CI engine is used for the study under different speed modes. All types of characteristics for various mixtures are estimated in running the engine. Pure diesel is indicated by B-0 and pure mahua bio-diesel is represented by B-100. From the test results, it is found that B-25 gives almost the same BTE as B-0 at maximum load, compared to all the blends. The blend B-0 and B-25 give the least SFC of 0.332 and 0.268 kg/kWh at minimum speed (1200 rpm) and maximum speed (2400 rpm) at maximum load as contrasted to all mixtures. The B-100 gave 3.01% of NOx while related to B-0 @ lower speed

Depletion of Fumarate Hydratase, an Essential TCA Cycle Enzyme, Drives Proliferation in a Two-Step Model

Fumarate hydratase (FH) is an evolutionary conserved TCA cycle enzyme that reversibly catalyzes the hydration of fumarate to L-malate and has a moonlight function in the DNA damage response (DDR). Interestingly, FH has a contradictory cellular function, as it is pro-survival through its role in the TCA cycle, yet its loss can drive tumorigenesis. Here, we found that in both non-cancerous (HEK-293T) and cancerous cell lines (HepG2), the cell response to FH loss is separated into two distinct time frames based on cell proliferation and DNA damage repair. During the early stages of FH loss, cell proliferation rate and DNA damage repair are inhibited. However, over time the cells overcome the FH loss and form knockout clones, indistinguishable from WT cells with respect to their proliferation rate. Due to the FH loss effect on DNA damage repair, we assumed that the recovered cells bear adaptive mutations. Therefore, we applied whole-exome sequencing to identify such mutated genes systematically. Indeed, we identified recurring mutations in genes belonging to central oncogenic signaling pathways, such as JAK/STAT3, which we validated in impaired FH-KO clones. Intriguingly, we demonstrate that these adaptive mutations are responsible for FH-KO cell proliferation under TCA cycle malfunction

Overexpression of UBA5 in Cells Mimics the Phenotype of Cells Lacking UBA5

Ufmylation is a posttranslational modification in which the modifier UFM1 is attached to target proteins. This conjugation requires the concerted work of three enzymes named UBA5, UFC1, and UFL1. Initially, UBA5 activates UFM1 in a process that ends with UFM1 attached to UBA5’s active site Cys. Then, in a trans-thiolation reaction, UFM1 is transferred from UBA5 to UFC1, forming a thioester bond with the latter. Finally, with the help of UFL1, UFM1 is transferred to the final destination—a lysine residue on a target protein. Therefore, not surprisingly, deletion of one of these enzymes abrogates the conjugation process. However, how overexpression of these enzymes affects this process is not yet clear. Here we found, unexpectedly, that overexpression of UBA5, but not UFC1, damages the ability of cells to migrate, in a similar way to cells lacking UBA5 or UFC1. At the mechanistic level, we found that overexpression of UBA5 reverses the trans-thiolation reaction, thereby leading to a back transfer of UFM1 from UFC1 to UBA5. This, as seen in cells lacking UBA5, reduces the level of charged UFC1 and therefore harms the conjugation process. In contrast, co-expression of UBA5 with UFM1 abolishes this effect, suggesting that the reverse transfer of UFM1 from UFC1 to UBA5 depends on the level of free UFM1. Overall, our results propose that the cellular expression level of the UFM1 conjugation enzymes has to be tightly regulated to ensure the proper directionality of UFM1 transfer

Lactational Exposure to Di-2-ethyl Hexyl Phthalate (Dehp) Induces Oxidative Stress and Causes Neurodegeneration in Hippocampus of Offspring Female Albino Rats

The purpose of this study was to determine the effect of DEHP on the hippocampus of F1 progeny female albino rats. Healthy mother rats were divided into four groups. The first group (control) was orally fed with olive oil–vehicle and the other three groups were treated with DEHP 1, 10 and 100 mg /kg bw/day via oral gavage from PND (Post natal day) 1 till 21. On PND 60 the offspring female rats were sacrificed, their hippocampus dissected and processed for biochemical analysis. Results showed that DEHP induced oxidative stress in hippocampus by increasing reactive oxygen species and decreasing antioxidant enzymes. Further, DEHP reduced the mRNA expression of ER?, ? and decreased that of Bcl2. Construction of a protein-protein interaction map with ER?, ?, Bcl2 and their downstream interacting partners confirmed the existence of a network, enriched for molecular functions. To conclude, lactational exposure to DEHP causes hippocampal neurotoxicity.&nbsp